by Alzheimer’s disease is an incurable brain disease that leads to dementia and ultimately death. It affects millions of people worldwide and puts a heavy toll on economies, with estimated costs accounting for one percent of the global gross domestic product. The disease is characterized by the accumulation and aggregation of misfolded amyloid-beta peptides (Aβ peptides) in the brain, which triggers harmful processes in the neurons, resulting in loss of vital cell functions and brain function.
Researchers at Chalmers University of Technology in Sweden have made an important breakthrough in the field of Alzheimer’s research. They have demonstrated that the use of graphene oxide nanoflakes can reduce the toxicity associated with the accumulation of amyloid-beta peptides in yeast cells. While previous studies have shown the potential of graphene oxide in reducing the toxicity of protein aggregates, this study is the first to demonstrate its effectiveness in yeast cells.
The researchers used a yeast cell model that closely mimics the neurons affected by Alzheimer’s disease in humans. They found that treatment with graphene oxide led to reduced levels of aggregated amyloid-beta peptides in the yeast cells. The mechanism behind this effect involves the alteration of cell metabolism, which increases the cells’ capacity to cope with misfolded proteins and oxidative stress.
Proteins and peptides, which are made up of amino acids, can become deformed if they fold incorrectly during formation in the cell. When amyloid-beta peptides accumulate in the brain, they form aggregates that are classified as proteins. These aggregates exert neurotoxic effects on the neurons, causing various cellular metabolic disorders and increased oxidative stress.
The researchers conducted their study using a combination of protein analysis and follow-up experiments. They used baker’s yeast as an in vivo model for human cells, as both cell types have similar systems for controlling protein quality. The yeast cells used in the study have characteristics that resemble neurons affected by amyloid-beta peptide accumulation, including endoplasmic reticulum stress, mitochondrial dysfunction, and elevated production of reactive oxygen radicals.
Graphene oxide nanoflakes are two-dimensional carbon nanomaterials that possess unique properties, such as outstanding conductivity and high biocompatibility. They are widely used in various research projects, including the development of cancer treatments, drug delivery systems, and biosensors. When graphene oxide enters living cells, it interacts with biomolecules, such as proteins, and interferes with their self-assembly processes.
Graphene oxide nanoflakes act by preventing the accumulation of amyloid-beta peptides and promoting the disintegration of existing aggregates. The researchers believe that graphene oxide acts through two independent pathways to mitigate the toxic effects of amyloid-beta peptides in yeast cells. It directly prevents accumulation and indirectly activates specific genes for stress response, increasing the cells’ ability to handle misfolded proteins and oxidative stress.
This groundbreaking study opens up new possibilities for research in the field of neurodegenerative diseases. The researchers have also shown that graphene oxide reduces the toxic effects of protein aggregates associated with Huntington’s disease in a yeast model. The next step is to investigate whether graphene oxide can be developed into a drug delivery system for Alzheimer’s disease. Additionally, the researchers aim to explore the potential beneficial effects of graphene oxide in other neurodegenerative diseases, such as Parkinson’s disease.
Overall, this research highlights the potential of graphene oxide as a nano-solution to reduce the toxicity associated with Alzheimer’s proteins. It offers hope for the development of effective strategies to treat Alzheimer’s disease and other neurodegenerative disorders in the future.
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1. Source: Coherent Market Insights, Public sources, Desk research
2. We have leveraged AI tools to mine information and compile it
